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Associated professor Masyuta D.I.

M.Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A.V., Ph.D. RESPIRATORY FAILURE IN CHILDREN. Associated professor Masyuta D.I. RESPIRATORY FAILURE. Respiratory failure is defined by alterations in the arterial PO 2 and PCO 2 .

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Associated professor Masyuta D.I.

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  1. M.Gorky Donetsk National Medical UniversityDepartment No. 2 of PediatricsHead of the Department Dr. Churilina A.V., Ph.D.RESPIRATORY FAILURE IN CHILDREN Associated professor Masyuta D.I.

  2. RESPIRATORY FAILURE • Respiratory failure is defined by alterations in the arterial PO2 and PCO2. • This approach is convenient because blood gas analysis is readily available and easy to interpret. • In addition, arterial PO2 and PCO2 are tightly regulated by the central nervous system based on the information provided by a complex system of sensors; consequently alterations in their values usually indicate that the mechanisms that execute the regulation are either overwhelmed by the disease or have failed.

  3. ETIOLOGY • Frequently, acute respiratory failure occurs in patients who are known to have mild to moderately severe chronic pulmonary disease with normal arterial carbon dioxide tension.During an intercurrent acute illness (e.g., RSV, influenza), such a patient may deteriorate rapidly and develop hypercapnia.

  4. ETIOLOGY • Previously well children may also develop acute respiratory failure as a result of • pneumonia, • epiglottitis or other cause of upper airway obstruction, • status asthmaticus, • aspiration (including near-drowning), • multisystem organ dysfunction with the adult respiratory distress syndrome, • severe heart failure, or other causes of pulmonary edema, and • certain poisonings.

  5. ETIOLOGY • Patients with cystic fibrosis, bronchopulmonary dysplasia (BPD), or severe scoliosis often develop acute respiratory failure following surgery. • Acute central nervous system disease may cause respiratory failure by interfering with the central control of breathing. • Severe muscle disease and thoracic abnormalities may result in respiratory failure because of inadequate alveolar ventilation.

  6. CLINICAL MANIFESTATIONS • The limited ability of the developing respiratory system to compensate for disease-induced mechanical abnormalities makes the early recognition of respiratory failure essential. • Respiratory failure should be anticipated rather than recognized so that alterations in gas exchange can be prevented.

  7. CLINICAL MANIFESTATIONS • During physical examination, the clinician should avoid interfering with the patient's own mechanisms of compensation. • An awake child with upper airway obstruction caused by croup or epiglottitis, for instance, may be more stable in a mother's arms because the increased gas flows generated during crying make breathing mechanically inefficient and can precipitate failure. • Similarly, most patients with severe restrictive and obstructive disease tolerate the supine position poorly because the weight of the abdominal organs imposes an additional burden on the diaphragm.

  8. CLINICAL MANIFESTATIONS • The physical examination is useful in the evaluation of children with respiratory disease. • In a child suspected of respiratory failure, this evaluation should always start with a quick assessment of the adequacy of ventilation.

  9. CLINICAL MANIFESTATIONS • This assessment includes • the presence and vigor of the respiratory movements, • breathing rate, • extent of the respiratory movements, • the presence of cyanosis, and • the presence of signs of upper airway obstruction. • A child with grossly inadequate respiratory efforts or complete airway obstruction will not survive long unless ventilation of the lungs is restored immediately.

  10. CLINICAL MANIFESTATIONS • In addition, special attention must be paid to the patient's state of consciousness. • Hypoxemia and hypercarbia frequently cause lethargy and confusion alternating with agitation. • Whether resulting from these or other concurrent mechanisms, central nervous system depression requires immediate attention because it further limits the ability of the respiratory system to deal with mechanical loads and leaves the airway unprotected against obstruction and aspiration of foreign materials.

  11. CLINICAL MANIFESTATIONS • The patient is usually hyperpneic and cyanotic, and may use the accessory muscles of respiration; most sit up and lean forward to improve leverage for the accessory muscles and to allow easy diaphragmatic movement. • Symptoms and signs of the underlying disease are also present.

  12. CLINICAL MANIFESTATIONS • Acute hypoxemia and hypercapnia result in dilatation of the cerebral blood vessels and increased blood flow, often accompanied by severe headache. • The sudden increased work of the accessory muscles of breathing may result in severe lower back pain. • Although moderate to severe hypercapnia can cause peripheral vasodilatation, mild to moderate hypoxemia can cause peripheral vasoconstriction, and the patient may complain of cold extremities. • Other symptoms of hypoxia include restlessness, dizziness, and impaired thought.

  13. CLINICAL MANIFESTATIONS • Acute respiratory failure can also result in characteristic multisystem complications. These include • gastrointestinal hemorrhage ("stress" ulcer), • cardiac arrhythmias (supraventricular arrhythmias), • renal failure, and • malnutrition.

  14. DIAGNOSIS • A PaCO2 of over 40 mm Hg suggests the possibility of developing acute respiratory failure, and a PaCO2 of 50 mm Hg or higher suggests it is imminent. • Most patients with acute hypercapnia also have a PaO2 below 55 mm Hg in room air, suggesting that the oxygen content of the blood may be inadequate to meet the normal needs of the vital organs. • Furthermore, at PaCO2 levels above 54 mm Hg, diaphragmatic function may be impaired, accelerating the patient's decline.

  15. TREATMENT • The goal of treatment of respiratory failure is the restoration of adequate gas exchange with a minimum of complications. • This is achieved by eliminating as quickly as possible the initiating factors.

  16. TREATMENT • Specific therapy of the initiating and/or underlying disease is essential. • Thus respiratory failure caused by cardiogenic pulmonary edema is treated with inotropic medications and diuretics. • The child with asthma should be managed with bronchodilators and anti-inflammatory medications. • Unfortunately, even in acute illnesses such as these, the response to the treatment is not immediate and frequently the entire function of the respiratory system must be artificially supported.

  17. OXYGEN THERAPY • Hypoxemia is more dangerous than hypercarbia and may be easier to correct. • Administration of supplemental oxygen is a safe and wise precaution in all patients at risk for respiratory failure, even if there is no initial evidence of hypoxemia. • Oxygen can be administered with • face masks, • nasal cannulas, • hoods, or • tents.

  18. OXYGEN THERAPY • Face masks are usually not well tolerated by frightened infants and children. • Hoods provide more consistent inspired oxygen concentrations than any other device, but they are bulky and limit access to the patient. • For this reason, they have limited applicability in the initial treatment in the emergency room.

  19. VENTILATORY SUPPORT • The indication for ventilatory support in a child with respiratory failure is usually based on the persistence or worsening of gas exchange abnormalities. • Mechanical ventilation is necessary in a child with pneumonia who develops severe hypoxemia and hypercarbia because even the most effective antibiotic therapy requires time.

  20. VENTILATORY SUPPORT • On occasion, ventilatory support must be instituted in the absence of alterations in the arterial PCO2 and PCO2 when the dysfunction of other systems places gas exchange at jeopardy by severely limiting the compensatory ability of the respiratory system. • Cardiovascular shock is a typical example. In this condition, decreased blood flow and substrate delivery to the respiratory muscles may reduce the force that these muscles can develop and can precipitate respiratory failure, even in the absence of substantial mechanical abnormalities of the respiratory system.

  21. VENTILATORY SUPPORT • Ventilatory support usually (but not always) requires intubation of the trachea with an endotracheal tube or less often a tracheostomy cannula. • Regardless of the type of ventilator, the objective of mechanical ventilation is not to normalize arterial blood gas tensions but rather to provide "adequate" gas exchange.

  22. VENTILATORY SUPPORT • The definition of what is "adequate" has changed substantially. • At present, there is reasonable consensus among those treating critically ill children that some degree of hypercarbia and hypoxemia is acceptable in order to minimize oxygen- and stretch-induced lung injury.

  23. VENTILATORY SUPPORT • Moderate (permissive) hypercarbia (PCO2 60–80 mm Hg) has no detectable negative consequences over short periods of time, in part because its effects on the arterial pH are reduced through renal retention of bicarbonate. • Moderate hypoxemia (oxygen saturation 85–90%) is similarly well tolerated in otherwise stable patients, particularly if the hemoglobin concentration and the cardiac output are maintained at physiological values and conditions such as fever and agitation, which increase tissue oxygen demands, are avoided.

  24. VENTILATORY SUPPORT • Artificial-mechanical ventilation is usually initiated with conventional volume-driven ventilators. • High frequency jet or oscillator ventilators are often used as rescue therapy if conventional ventilators fail to improve oxygenation.

  25. EXTRACORPOREAL MEMBRANE OXYGENATION • Extracorporeal membrane oxygenation (ECMO) and/or carbon dioxide removal is employed in the treatment of • newborns and small infants with life-threatening, • refractory respiratory failure that is unresponsive to mechanical ventilation and is expected to resolve in a short period of time.

  26. EXTRACORPOREAL MEMBRANE OXYGENATION • ECMO uses an artificial membrane to regulate the oxygen and carbon dioxide content of blood diverted from the patient's central veins. • The treated blood is then returned with the help of an artificial pump to the arterial (veno-arterial) or venous (veno-venous) circulation.

  27. EXTRACORPOREAL MEMBRANE OXYGENATION • Because of its risks (from vascular cannulation and anticoagulation) and the fact that its benefits over conventional management in non-neonatal patients have not been unequivocally demonstrated, indications for extracorporeal gas exchange should be contemplated with a great deal of caution. • Inhaled nitric oxide may acutely improve oxygenation by reducing increased pulmonary vascular resistance.

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